The purpose of this study is to elucidate some of the important gaps in our knowledge concerning the biochemical mechanisms involved in the pathogenesis of human bronchial asthma. Projected studies include: 1) further attempts to elucidate the basis for the acquired alteration in adrenergic responsiveness seen in individuals with severe persistent asthma; 2) determination of the structure and mechanism of biosynthesis and degradation of ECF-A and SRS-A, two of the putative mediators in the allergic form of the disease; 3) the development of sensitive methods for measuring ECF-A and SRS-A and their application to clinical specimens; 4) detailed studies of prostaglandin metabolism in an attempt to elucidate the role of these or related structures in the pathogenesis of asthma, particularly the form that is exacerbated by analgesic agents.